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The effects of home-based exercise therapy for breast cancer-related fatigue induced by radical radiotherapy.
Mavropalias, G, Cormie, P, Peddle-McIntyre, CJ, Galvão, DA, Taaffe, DR, Schofield, C, Ray, S, Zissiadis, Y, Newton, RU
Breast cancer (Tokyo, Japan). 2023;30(1):139-150
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Breast cancer (BCa) is the most common form of cancer among women. Radiotherapy (RT) treatment is an important component of breast cancer treatment and is used with curative intent as well as for palliation. One commonly reported adverse side effect of RT is cancer related fatigue (CRF). The aims of this study were to (a) examine the effects of a 12-week home-based resistance and aerobic exercise program on CRF, health-related quality of life (HRQoL), and sleep quality and duration in BCa patients during and up to 12 months after RT, and (b) investigate how CRF, HRQoL, and sleep quality and duration affect the participants’ ability to follow their prescribed exercise program. This study was a two-arm, randomised controlled clinical trial. One hundred and six (n = 106) women with stage I-III BCa scheduled to receive radical RT were randomised into exercise (n = 51) or usual care (n = 55). Results show that CRF was present at baseline and persisted during RT. The exercise group had a quicker reduction in CRF compared to the usual care group. Moreover, there was a significant difference in the HRQoL during RT between groups, and a quicker HRQoL improvement post-RT for the exercise group, with no changes in sleep quality or duration. Additionally, less fatigue and less trouble sleeping were associated with greater weekly aerobic exercise duration and higher rating of perceived exertion during aerobic exercise. Authors conclude that home-based exercise during RT is safe and effective in reducing CRF and improving HRQoL
Abstract
BACKGROUND Radiotherapy (RT) can lead to cancer-related fatigue (CRF) and decreased health-related quality of life (HRQoL) in breast cancer patients. The purpose of this trial was to examine the feasibility and efficacy of a home-based resistance and aerobic exercise intervention for reducing CRF and improving HRQoL in breast cancer patients during RT. METHODS Women with breast cancer (N = 106) commencing RT were randomized to 12 weeks of home-based resistance and aerobic exercise (EX) or usual care/control (CON). The primary endpoint was CRF, with secondary endpoints of HRQoL, sleep duration and quality, and physical activity. Measurements were undertaken prior to RT, at completion of RT (~ 6 weeks), at completion of the intervention (12 weeks), and 6 and 12 months after RT completion, while CRF was also measured weekly during RT. RESULTS Eighty-nine women completed the study (EX = 43, CON = 46). Over the 12-week intervention, EX completed 1-2 resistance training sessions and accumulated 30-40 min of aerobic exercise weekly. For CRF, EX had a quicker recovery both during and post-RT compared to CON (p < 0.05). Moreover, there was a significant difference in HRQoL between groups at RT completion, with HRQoL unchanged in CON and higher in EX (p < 0.05). There was no change in sleep duration or quality for either group and there were no exercise-related adverse effects. CONCLUSIONS Home-based resistance and aerobic exercise during RT is safe, feasible, and effective in accelerating CRF recovery and improving HRQoL. Improvements in CRF and HRQoL for these patients can be achieved with smaller exercise dosages than stated in the generic recommendations for breast cancer.
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Effects of acute sleep loss on leptin, ghrelin, and adiponectin in adults with healthy weight and obesity: A laboratory study.
van Egmond, LT, Meth, EMS, Engström, J, Ilemosoglou, M, Keller, JA, Vogel, H, Benedict, C
Obesity (Silver Spring, Md.). 2023;31(3):635-641
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A lack of sleep may be a risk factor for weight gain. Leptin is an adipocyte-derived hormone that activates satiety networks within the brain. Ghrelin, as opposed to leptin, is mainly produced by the stomach and it acts as a hunger hormone, signalling fuel status to the central nervous system. Some studies have found either no alterations or higher leptin and lower ghrelin blood levels following experimental sleep deprivation. The aim of this study was to investigate whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner. This study is a laboratory study based on blood samples from 44 participants, mainly university students. Results show that: - acute total sleep deprivation is linked to lower serum levels of the adipokine leptin and higher blood levels of ghrelin. - following sleep deprivation, serum adiponectin levels were elevated. - the drop in serum leptin was larger in women after total sleep deprivation; however, there wasn’t a significant association between biological sex and experimental condition. - the increase in blood levels of adiponectin was slightly more pronounced among women, whereas there weren’t any differences in the effects of sleep loss on plasma ghrelin. Authors conclude that acute total sleep deprivation shifts the endocrine balance from the satiety hormone leptin toward the hunger-promoting hormone ghrelin. However, further investigation in larger samples focusing on their findings linked to sex- and weight-specific differences in leptin, ghrelin, and adiponectin are needed.
Expert Review
Conflicts of interest:
None
Take Home Message:
Sleep deprivation may shift the balance of appetite controlling hormones causing an increase in hunger and decreased satiety and therefore resulting in increased food intake. These changes may be more pronounced in biological females.
Evidence Category:
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A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Introduction
Sleep deprivation may contribute to weight gain and obesity through its effect on the hormonal pathways promoting hunger and satiety. Research has also linked chronic sleep loss with an increase in the brain reward response to food, thus driving an increase in daily food intake. Leptin and ghrelin are hormones involved in the control of food intake. Some research has associated alterations in these hormones following sleep loss, whilst others have not.
This study aimed to investigate whether biological sex and weight status affect fasting serum levels of leptin, ghrelin and adiponectin following chronic sleep deprivation in a supervised laboratory setting.
Methods
This randomised crossover design study included n=44 mixed sex participants with a mean age of 24.9 years. A total of 19 of the participants were classed as obese, with the remaining n= 25 participants were considered normal weight. Participants completed 2 nights in experimental sessions under continuously supervised conditions in a laboratory. One night was spent awake and the other asleep. Fasting blood samples were taken the morning after each session to measure levels of leptin, ghrelin and adiponectin.
Results
Serum levels of leptin after one night’s sleep loss were around 7% lower than those measured after sleep (17.3 = +/-2.6 vs 18.6 +/- 2.8 ng/mL, p = 0.037). Adjustments using sex-stratified analysis showed significantly lower levels of serum leptin in women (25.8 +/_4.3 vs 28.1 +/_ 4.7 ng/mL, p = 0.030) but not for men (10.1 +/_ 2.4 vs 10.6 +/_ 2.3 ng/mL, p = 0.458). However, when comparing individual participant differences between sleep and wake sessions, the results were not significant. Additionally, no significant differences were found between normal weight and obese participants.
Higher levels of ghrelin were found following sleep deprivation in both sexes and weight sub-groups (839.4 +/-77.5 vs 741.4+/-63.2 pg/mL, p= 0.003). Adiponectin was also found to be elevated in all participants regardless of biological sex or weight status (7.5 +/- 0.6 vs 6.8 +/- 0.6ug/mL, p= 0.003). However, ghrelin was observed to increase slightly more in participants with obesity, whereas elevations in adiponectin were slightly greater in those of normal weight.
Conclusion
In this study, sleep loss was associated with lowered levels of leptin and higher levels of ghrelin. Analysis between biological sexes indicated that there may be a greater decrease in leptin in females. Serum levels of adiponectin were also found to be elevated after sleep deprivation for both sexes with a slightly larger increase in women. These changes may result in increased hunger and food intake and decreased satiety. No significant differences were found between normal weight and obese participants.
Notes: The authors reported no conflicts of interest.
Clinical practice applications:
Sleep deprivation may lead to lower levels of leptin in both sexes with a greater decrease for females. Ghrelin and adiponectin levels may be increased in both men and women after sleep loss with a slightly larger increase in adiponectin for women. This could lead to an increase in appetite, food consumption and therefore weight gain, particularly in women.
Considerations for future research:
- Larger studies are needed to investigate sex and weight status related differences in serum levels of ghrelin, leptin and adiponectin.
- It may be beneficial for blood samples to be taken at different points during the day to allow for fluctuations in hormone levels.
- Food intake should be measured to monitor any increases in food intake.
Abstract
OBJECTIVE This study investigated whether blood concentrations of leptin, ghrelin, and adiponectin are affected by acute total sleep deprivation in a sex- and weight-specific manner. METHODS A total of 44 participants (mean age 24.9 years; 20 women; 19 with obesity) participated in a crossover design, including one night of sleep deprivation and one night of sleep in the laboratory. After each night, fasting blood was collected. RESULTS After sleep deprivation, fasting levels of leptin were lower (mean [SE], vs. sleep: 17.3 [2.6] vs. 18.6 [2.8] ng/mL), whereas those of ghrelin and adiponectin were higher (839.4 [77.5] vs. 741.4 [63.2] pg/mL and 7.5 [0.6] vs. 6.8 [0.6] μg/mL, respectively; all p < 0.05). The changes in leptin and adiponectin following sleep loss were more pronounced among women. Furthermore, the ghrelin increase was stronger among those with obesity after sleep loss. Finally, the sleep loss-induced increase in adiponectin was more marked among normal-weight participants. CONCLUSIONS Acute sleep deprivation reduces blood concentrations of the satiety hormone leptin. With increased blood concentrations of ghrelin and adiponectin, such endocrine changes may facilitate weight gain if persisting over extended periods of sleep loss. The observed sex- and weight-specific differences in leptin, ghrelin, and adiponectin call for further investigation.
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How do previously inactive individuals restructure their time to 'fit in' morning or evening exercise: a randomized controlled trial.
Brooker, PG, Gomersall, SR, King, NA, McMahon, NF, Leveritt, MD
Journal of behavioral medicine. 2023;46(3):429-439
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The number of hours in a day is fixed and finite, distributed between obligatory time (such as time spent working, sleeping, domestic activities, commuting or eating) and discretionary time (the remaining ‘free’ time). The way individuals restructure the timing of their behaviours can influence the effectiveness of exercise, and have important health consequences, depending on what activities are displaced. The aim of this study was to investigate how previously inactive adults restructure their time when they undertake morning or evening exercise. This study was conducted within a larger randomised controlled trial which used a three-armed, randomised controlled trial design, with a 12-week lifestyle intervention. Participants (n = 100) were randomized into one of two intervention groups, or a waitlist control group at a 2:2:1 ratio. Results showed that time spent engaging in physical activity was significantly increased from baseline at both mid- and post-intervention for both intervention groups. Furthermore, participants in both intervention groups reported more time spent sleeping, and less time watching television/playing videogames. Authors conclude that the time for exercise was largely drawn from a discretionary time (watching TV), and the patterns of change in time use was similar when exercise was performed in the morning compared with the evening.
Abstract
The objective of this study was to investigate changes in sedentary and active behaviors when previously inactive adults start exercising in the morning or evening. One-hundred adults with overweight or obesity (BMI ≥ 25 kg/m2) were recruited for a 12-week intervention and randomized to one of three groups: (i) morning exercise (AMEx; 0600-0900); (ii) evening exercise (PMEx; 1600-1900); or (iii) waitlist control. AMEx and PMEx were prescribed self-paced aerobic exercise to achieve a weekly total of 250 min via a combination of supervised and unsupervised training. Sedentary and active behavior times were measured at baseline, mid- and post-intervention using the multimedia activity recall for children and adults. Time spent engaging in physical activity was significantly increased from baseline at both mid- (+ 14-22 min·day-1) and post-intervention (+ 12-19 min·day-1), for AMEx and PMEx. At 12-weeks, participants in both morning and evening exercise groups reported increased time spent Sleeping (+ 36 and + 20 min·day-1, respecitively), and reduced time spent watching TV/playing videogames (- 32 and - 25 min·day-1, respectively). In response to an exercise stimulus, previously inactive adults make encouraging modifications in how they use their time, and the patterns of change are similar with morning and evening exercise.
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Time of the day of exercise impact on cardiovascular disease risk factors in adults: a systematic review and meta-analysis.
Sevilla-Lorente, R, Carneiro-Barrera, A, Molina-Garcia, P, Ruiz, JR, Amaro-Gahete, FJ
Journal of science and medicine in sport. 2023;26(3):169-179
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In humans, shifted sleep patterns seem to interfere with several metabolic pathways. Shift work, short sleep duration, exposure to artificial light, inadequate eating time window, and lack of physical activity, are some characteristics of the modern lifestyle that contributes to the occurrence and worsening of cardiovascular disease (CVD). The aim of this study was to analyse the time of the day of exercise-induced effects on CVD risk factors in adults. This study was a systematic review and meta-analysis of twenty-two studies. Results showed that exercise produces an acute reduction of systolic blood pressure independently of the time of the day at which it is performed. Similarly, exercise produces an acute increase in blood glucose independently of the time of the day. Authors concluded that further research is needed to establish whether there is a diurnal variation of exercise on cardiovascular health and how it is related to health status, sex, or the type of exercise.
Abstract
OBJECTIVES To compare the effect of a single bout of morning vs. evening exercise on cardiovascular risk factors in adults. DESIGN Systematic review and meta-analysis. METHODS A systematic search of studies was conducted using PubMed and Web of Science from inception to June 2022. Selected studies accomplished the following criteria: crossover design, acute effect of exercise, blood pressure, blood glucose, and/or blood lipids as the study's endpoint, a washout period of at least 24 h, and adults. Meta-analysis was performed by analyzing: 1) separated effect of morning and evening exercise (pre vs. post); and 2) comparison between morning and evening exercise. RESULTS A total of 11 studies were included for systolic and diastolic blood pressure and 10 studies for blood glucose. Meta-analysis revealed no significant difference between morning vs. evening exercise for systolic blood pressure (g ∆ = 0.02), diastolic blood pressure (g ∆ = 0.01), or blood glucose (g ∆ = 0.15). Analysis of moderator variables (age, BMI, sex, health status, intensity and duration of exercise, and hour within the morning or evening) showed no significant morning vs. evening effect. CONCLUSIONS Overall, we found no influence of the time of the day on the acute effect of exercise on blood pressure neither on blood glucose.
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Association of meal timing with body composition and cardiometabolic risk factors in young adults.
Dote-Montero, M, Acosta, FM, Sanchez-Delgado, G, Merchan-Ramirez, E, Amaro-Gahete, FJ, Labayen, I, Ruiz, JR
European journal of nutrition. 2023;62(5):2303-2315
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Despite the known consequences of excess body weight, the prevalence of obesity continues to rise. Body weight regulation and obesity are highly influenced by several factors such as genetics, physiology, and socioeconomic factors. The aim of this study was to elucidate the association of meal timing with anthropometry body composition and cardiometabolic risk factors in young adults. This study was a cross-sectional study of 118 young adults (n=82 women). Results showed that meal timing is not related to anthropometry or body composition parameters in young adults. Similarly, caloric midpoint, eating jetlag and the time from last food intake to midsleep point are not associated with cardiometabolic risk factors. However, a longer daily eating window and a shorter time from midsleep point to first food intake (i.e., earlier first food intake in a 24 h cycle) are associated with a healthier cardiometabolic profile in young men. Authors concluded that eating early in alignment with circadian rhythms may improve cardiometabolic health.
Abstract
PURPOSE To investigate the association of meal timing with body composition and cardiometabolic risk factors in young adults. METHODS In this cross-sectional study participated 118 young adults (82 women; 22 ± 2 years old; BMI: 25.1 ± 4.6 kg/m2). Meal timing was determined via three non-consecutive 24-h dietary recalls. Sleep outcomes were objectively assessed using accelerometry. The eating window (time between first and last caloric intake), caloric midpoint (local time at which ≥ 50% of daily calories are consumed), eating jetlag (variability of the eating midpoint between non-working and working days), time from the midsleep point to first food intake, and time from last food intake to midsleep point were calculated. Body composition was determined by DXA. Blood pressure and fasting cardiometabolic risk factors (i.e., triglycerides, total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and insulin resistance) were measured. RESULTS Meal timing was not associated with body composition (p > 0.05). The eating window was negatively related to HOMA-IR and cardiometabolic risk score in men (R2 = 0.348, β = - 0.605; R2 = 0.234, β = - 0.508; all p ≤ 0.003). The time from midsleep point to first food intake was positively related to HOMA-IR and cardiometabolic risk score in men (R2 = 0.212, β = 0.485; R2 = 0.228, β = 0.502; all p = 0.003). These associations remained after adjusting for confounders and multiplicity (all p ≤ 0.011). CONCLUSIONS Meal timing seems unrelated to body composition in young adults. However, a longer daily eating window and a shorter time from midsleep point to first food intake (i.e., earlier first food intake in a 24 h cycle) are associated with better cardiometabolic health in young men. CLINICAL TRIAL REGISTRATION NCT02365129 ( https://www. CLINICALTRIALS gov/ct2/show/NCT02365129?term=ACTIBATE&draw=2&rank=1 ).
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Causal relationship between nonalcoholic fatty liver disease and different sleep traits: a bidirectional Mendelian randomized study.
Sun, Z, Ji, J, Zuo, L, Hu, Y, Wang, K, Xu, T, Wang, Q, Cheng, F
Frontiers in endocrinology. 2023;14:1159258
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Non-alcoholic fatty liver disease (NAFLD) is caused by a build up of fat in the liver. NAFLD is becoming more common, with the rise in rates of obesity. There are no specific medications available for NAFLD and patients are advised to manage their diets and lifestyle following diagnosis. The aim of this study was to assess and evaluate the causal relationship between sleep and NAFLD. The study was a two-way Mendelian randomised clinical trial. Results showed that different sleep traits can be the cause of the onset and exacerbation of NAFLD. NAFLD does not change sleep traits and the causal relationship between them is unidirectional. Authors conclude that sleep characteristics are associated with an elevated risk of NAFLD. Thus, enhancing sleep should be considered by healthcare practitioners as part of prevention and management NAFLD.
Abstract
BACKGROUND AND AIMS Non-alcoholic fatty liver disease(NAFLD) is common worldwide and has previously been reported to be associated with sleep traits. However, it is not clear whether NAFLD changes sleep traits or whether the changes in sleep traits lead to the onset of NAFLD. The purpose of this study was to investigate the causal relationship between NAFLD and changes in sleep traits using Mendelian randomization. METHODS We proposed a bidirectional Mendelian randomization (MR) analysis and performed validation analyses to dissect the association between NAFLD and sleep traits. Genetic instruments were used as proxies for NAFLD and sleep. Data of genome-wide association study(GWAS) were obtained from the center for neurogenomics and cognitive research database, Open GWAS database and GWAS catalog. Three MR methods were performed, including inverse variance weighted method(IVW), MR-Egger, weighted median. RESULTS In total,7 traits associated with sleep and 4 traits associated with NAFLD are used in this study. A total of six results showed significant differences. Insomnia was associated with NAFLD (OR(95% CI)= 2.25(1.18,4.27), P = 0.01), Alanine transaminase levels (OR(95% CI)= 2.79(1.70, 4.56), P =4.71×10-5) and percent liver fat(OR(95% CI)= 1.31(1.03,1.69), P = 0.03). Snoring was associated with percent liver fat (1.15(1.05,1.26), P =2×10-3), alanine transaminase levels (OR(95% CI)= 1.27(1.08,1.50), P =0.04).And dozing was associated with percent liver fat(1.14(1.02,1.26), P =0.02).For the remaining 50 outcomes, no significant or definitive association was yielded in MR analysis. CONCLUSION Genetic evidence suggests putative causal relationships between NAFLD and a set of sleep traits, indicating that sleep traits deserves high priority in clinical practice. Not only the confirmed sleep apnea syndrome, but also the sleep duration and sleep state (such as insomnia) deserve clinical attention. Our study proves that the causal relationship between sleep characteristics and NAFLD is the cause of the change of sleep characteristics, while the onset of non-NAFLD is the cause of the change of sleep characteristics, and the causal relationship is one-way.
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Sleep loss disrupts the neural signature of successful learning.
Guttesen, AÁV, Gaskell, MG, Madden, EV, Appleby, G, Cross, ZR, Cairney, SA
Cerebral cortex (New York, N.Y. : 1991). 2023;33(5):1610-1625
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Understanding how sleep disturbances impair learning and memory is increasingly important in modern society, where many people fail to regularly obtain an adequate amount of sleep. The aim of this study was to investigate the relationship between sleep-associated consolidation and next-day learning and how suppressing slow-wave activity (SWA) [during slow-wave sleep, electrical activity in the brain changes while the body relaxes into deep and restorative rest] contributes to this relationship. This study was a within-subjects (n = 30), crossover design which showed that sleep improved both memory retention and next-day learning however, there was no evidence of a relationship between these measures or with SWA. Furthermore, an absence of sleep disrupts the neural operations underpinning memory encoding, leading to suboptimal performance. Authors conclude that an extended lack of sleep might disrupt the ability to draw upon semantic knowledge when encoding novel associations, necessitating the use of more surface-based and ultimately suboptimal routes to learning.
Abstract
Sleep supports memory consolidation as well as next-day learning. The influential "Active Systems" account of offline consolidation suggests that sleep-associated memory processing paves the way for new learning, but empirical evidence in support of this idea is scarce. Using a within-subjects (n = 30), crossover design, we assessed behavioral and electrophysiological indices of episodic encoding after a night of sleep or total sleep deprivation in healthy adults (aged 18-25 years) and investigated whether behavioral performance was predicted by the overnight consolidation of episodic associations from the previous day. Sleep supported memory consolidation and next-day learning as compared to sleep deprivation. However, the magnitude of this sleep-associated consolidation benefit did not significantly predict the ability to form novel memories after sleep. Interestingly, sleep deprivation prompted a qualitative change in the neural signature of encoding: Whereas 12-20 Hz beta desynchronization-an established marker of successful encoding-was observed after sleep, sleep deprivation disrupted beta desynchrony during successful learning. Taken together, these findings suggest that effective learning depends on sleep but not necessarily on sleep-associated consolidation.
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Sleep disruption and activation of cellular inflammation mediate heightened pain sensitivity: a randomized clinical trial.
Irwin, MR, Olmstead, R, Bjurstrom, MF, Finan, PH, Smith, MT
Pain. 2023;164(5):1128-1137
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Sleep disturbance is associated with elevated levels of inflammation. Experimental studies have found that even a modest amount of sleep loss activates inflammatory processes. Experimental sleep disruption also induces alterations in sleep architecture including loss of slow wave or N3 sleep and loss of rapid eye movement sleep. The aim of this study was to clarify whether changes in the amount of N3 sleep and cellular inflammation mediate thermal pain sensitivity (i.e., heat pain threshold) in response to experimental sleep disruption. This study was a secondary analysis (assessor-blind) of a randomised controlled trial. The enrolled participants were randomised to 1 of 2 groups: 2 nights of undisturbed sleep (US) and 2 nights of sleep disruption or forced awakening (FA). Participants underwent 2 consecutive nights of US (or FA), followed by a 2-week washout interval in their home environment, and then completed 2 consecutive nights of the opposing sleep condition FA (or US). Results showed that in healthy adults, experimental disruption of sleep due to the administration of FA induced a significant decrease in heat pain threshold, as compared with responses after US. Experimental manipulation of sleep with FA also led to disturbance in sleep continuity and changes in sleep architecture, including loss of N3 sleep. Moreover, in the morning after FA, there was a robust activation of cellular inflammation Authors conclude that the differential loss of N3 sleep and increases in cellular inflammation may be important drivers of pain sensitivity in response to sleep disruption.
Abstract
Sleep loss heightens pain sensitivity, but the pathways underlying this association are not known. Given that experimental sleep disruption induces increases in cellular inflammation as well as selective loss of slow wave, N3 sleep, this study examined whether these mechanisms contribute to pain sensitivity following sleep loss in healthy adults. This assessor-blinded, cross-over sleep condition, single-site, randomized clinical trial enrolled 95 healthy adults (mean [SD] age, 27.8 [6.4]; female, 44 [53.7%]). The 2 sleep conditions were 2 nights of undisturbed sleep (US) and 2 nights of sleep disruption or forced awakening (FA, 8 pseudorandomly distributed awakenings and 200 minutes wake time during the 8-hour sleep opportunity), administered in a cross-over design after 2 weeks of washout and in a random order (FA-US; US-FA). Primary outcome was heat pain threshold (hPTH). Sleep architecture was assessed by polysomnography, and morning levels of cellular inflammation were evaluated by Toll-like receptor-4 stimulated monocyte intracellular proinflammatory cytokine production. As compared with US, FA was associated with decreases in the amount of slow wave or N3 sleep ( P < 0.001), increases in Toll-like receptor-4 stimulated production of interleukin-6 and tumor necrosis factor-α ( P = 0.03), and decreases in hPTH ( P = 0.02). A comprehensive causal mediation analysis found that FA had an indirect effect on hPTH by decreases in N3 sleep and subsequent increases in inflammation (estimate=-0.15; 95% confidence interval, -0.30 to -0.03; P < 0.05) with the proportion mediated 34.9%. Differential loss of slow wave, N3 sleep, and increases in cellular inflammation are important drivers of pain sensitivity after sleep disruption.Clinical Trials Registration: NCT01794689.
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The Emergency Medical Services Sleep Health Study: A cluster-randomized trial.
Patterson, PD, Martin, SE, Brassil, BN, Hsiao, WH, Weaver, MD, Okerman, TS, Seitz, SN, Patterson, CG, Robinson, K
Sleep health. 2023;9(1):64-76
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Severe mental and physical fatigue in shift work occupations is widespread, and workplace fatigue impacts a great majority of the Emergency Medical Services (EMS) clinician first responders. The hypothesis of this study was that education and training focused on sleep health and fatigue, delivered in an asynchronous manner and tailored to EMS shift workers, would result in improvements in sleep quality and a reduction in self-reported fatigue after a 3-month study interval. This study was a cluster-randomised, 2-arm randomised trial with a wait-list control group. EMS agencies (clusters) were randomised to either the intervention group or a wait-list control group. Results showed that intention-to-treat analyses revealed no differences in measures of sleep quality or fatigue at 3 months or 6 months follow-up. Per protocol analyses showed that the greater the number of education modules viewed, the greater the improvement in sleep quality and the greater the reduction in fatigue at 3-month follow-up. Authors conclude that the findings of this study may be useful to EMS administrators when designing fatigue risk management programmes.
Abstract
BACKGROUND Greater than half of emergency medical services (EMS) clinician shift workers report poor sleep, fatigue, and inadequate recovery between shifts. We hypothesized that EMS clinicians randomized to receive tailored sleep health education would have improved sleep quality and less fatigue compared to wait-list controls after 3 months. METHODS We used a cluster-randomized, 2-arm, wait-list control study design (clinicaltrials.gov identifier: NCT04218279). Recruitment of EMS agencies (clusters) was nationwide. Our study was powered at 88% to detect a 0.4 standard deviation difference in sleep quality with 20 agencies per arm and a minimum of 10 individuals per agency. The primary outcome was measured using the Pittsburgh Sleep Quality Index (PSQI) at 3-month follow-up. Our intervention was accessible in an online, asynchronous format and comprised of 10 brief education modules that address fatigue mitigation topics prescribed by the American College of Occupational Environmental Medicine. RESULTS In total, 36 EMS agencies and 678 individuals enrolled. Attrition at 3 months did not differ by study group (Intervention = 17.4% vs. Wait-list control = 18.2%; p = .37). Intention-to-treat analyses detected no differences in PSQI and fatigue scores at 3 months. Per protocol analyses showed the greater the number of education modules viewed, the greater the improvement in sleep quality and the greater the reduction in fatigue (p < .05). CONCLUSIONS While intention-to-treat analyses revealed no differences in sleep quality or fatigue at 3 months, per protocol findings identified select groups of EMS clinician shift workers who may benefit from sleep health education. Our findings may inform fatigue risk management programs.
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Sleep-Opt-In: A Randomized Controlled Pilot Study to Improve Sleep and Glycemic Variability in Adults With Type 1 Diabetes.
Martyn-Nemeth, P, Duffecy, J, Quinn, L, Steffen, A, Baron, K, Chapagai, S, Burke, L, Reutrakul, S
The science of diabetes self-management and care. 2023;49(1):11-22
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Insufficient sleep (insufficient total sleep time) and irregular sleep timing (variability in the occurrence of sleep within a 24-hour period) are increasingly recognized as important contributors to glycaemic control and variability in type 1 diabetes (T1D). The aims of this study were to evaluate the feasibility and acceptability of a sleep intervention (Sleep-Opt-In) targeted for adults with type 1 diabetes with short or irregular sleep and to examine the effects of Sleep-Opt-In on sleep duration and regularity, glucose indices, and patient-reported outcomes. This study was a randomised controlled parallel trial design. Participants (n=14) were randomly assigned to either the Sleep-Opt-In intervention or a Healthy Living attention control group. Results showed that: - Sleep-Opt-In was feasible and acceptable to the target population. - participants with objectively confirmed short or irregular sleep, sleep irregularity improved by 25 minutes on average, whereas sleep duration improved only negligibly (8 minutes). - the control group experienced an increase in sleep duration but no change in sleep regularity. Authors conclude that Sleep-Opt-In is feasible, acceptable, and promising for further evaluation to improve sleep duration or regularity, glucose parameters and important patient reported outcomes of diabetes distress, daytime sleepiness, fatigue and depressive mood in the T1D population.
Abstract
PURPOSE The purpose of this study was to evaluate the feasibility and acceptability of a technology-assisted behavioral sleep intervention (Sleep-Opt-In) and to examine the effects of Sleep-Opt-In on sleep duration and regularity, glucose indices, and patient-reported outcomes. Short sleep duration and irregular sleep schedules are associated with reduced glycemic control and greater glycemic variability. METHODS A randomized controlled parallel-arm pilot study was employed. Adults with type 1 diabetes (n = 14) were recruited from the Midwest and randomized 3:2 to the sleep-optimization (Sleep-Opt-In) or Healthy Living attention control group. Sleep-Opt-In was an 8-week, remotely delivered intervention consisting of digital lessons, sleep tracker, and weekly coaching phone calls by a trained sleep coach. Assessments of sleep (actigraphy), glucose (A1C, continuous glucose monitoring), and patient-reported outcomes (questionnaires for daytime sleepiness, fatigue, diabetes distress, and depressive mood) were completed at baseline and at completion of the intervention. RESULTS Sleep-Opt-In was feasible and acceptable. Those in Sleep-Opt-In with objectively confirmed short or irregular sleep demonstrated an improvement in sleep regularity (25 minutes), reduced glycemic variability (3.2%), and improved time in range (6.9%) compared to the Healthy Living attention control group. Patient-reported outcomes improved only for the Sleep-Opt-In group. Fatigue and depressive mood improved compared to the control. CONCLUSIONS Sleep-Opt-In is feasible, acceptable, and promising for further evaluation as a means to improve sleep duration or regularity in the population of people with type 1 diabetes.